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Background Environmental nontuberculous mycobacteria species that are not members of the M. tuberculosis complex, are ordinary inhabitants of a wide variety of environmental reservoirs and their role in human and animal diseases has been fully recognized. Even if spontaneous mycobacterial infections have been reported in a wide variety of reptiles, this is the first report of systemic fatal mycobacteriosis sustained by Mycobacterium goodii in a pet reptile. Case presentation An adult, wild caught (WC), male Kenyan sand boa (Eryx colubrinus loveridgei) age unknown, was presented for clinical examination due to decreased activity level, decreased appetite and diarrhea. Blood tests showed unreliable results. Coprologic exam showed a moderate to severe presence of flagellates. X rays and ultrasound showed moderate presence of air and faeces in the large intestine. The snake was hospitalized and oral metronidazole was chosen as antiprotozoal agent in association with subcutaneous warm fluids. The snake was discharged after 2 weeks therapy in good clinical condition. Faecal exam resulted negative. One month after, the snake was quickly hospitalized again because of a recrudescence of symptoms. Biochemistry showed severe increase of AST, ALT and biliary acids. Severe leucocytosis and moderate to severe anemia were highlighted. Ultrasound examination revealed a severe diffused alteration of the liver parenchyma and a fine needle aspiration was performed. The cytological diagnosis was mixed inflammation, with a numerous of unstained rod-shaped bacteria both inside macrophages and free in the sample. The snake’s condition rapidly deteriorated and euthanasia was performed. The histology of the coelomic organs confirmed a systemic mycobacteriosis. Real-time PCR identified the mycobacteria as Mycobacterium goodii. Conclusions Species from the genus Mycobacterium are among the most important micro-organism including the causative agents of tuberculosis. Even if the general incidence of disease in reptiles due to mycobacteria is comparatively low, they can serve as reservoirs of many ubiquitous mycobacteria species. Mycobacterium goodii is a rapidly growing non‐tuberculous mycobacterium that has recently been associated with severe infections in animals and humans. Although in this case the pathogenesis was not completely clear, we highlight the zoonotic risk of mycobacteriosis in exotic animals especially in WC specimens.

Introduction SARS-CoV-2 is a virus that causes a potentially deadly syndrome that affects especially the respiratory tract Kidney-transplanted patients are immunosuppressed and more susceptible to viral infections We have examined our transplantation activity to explore the future role of kidney transplantation from deceased and living donors in COVID-19 era Patients and Methods The activity of our transplant center of Naples (one of the two transplant centers in Campania, South Italy) continued during the COVID-19 pandemic We have analysed the kidney transplants carried out between March 9 and June 9, 2020, comparing these data with the numbers of procedures performed in the two previous years Moreover, we have considered the possibility of performing living donor transplants during a worldwide pandemic Results From March 9, 2020, when the Italian lockdown begun, till June 9, 2020, five kidney transplants have been performed at our transplant center in Naples, all from deceased donors The donors and the recipients have been screened for COVID-19 infection, and the patients, all asymptomatic, followed strict preventive measures and were fully informed about the risks of surgery and immunosuppression during a pandemic All the transplanted patients remained COVID negative during the follow-up The number of transplants performed has been constant compared to the same months of 2018 and 2019 In agreement with the patients, we decided to postpone living donor transplants to a period of greater control of the SARS-CoV-2 spread in Italy Conclusion Deceased donor kidney transplantation should continue, especially in a region with moderate risk, like Campania, with a more careful selection of donors and recipients, preferring standard donors and recipients without severe comorbidities Living donor transplantation program, instead, should be postponed to a period of greater control of the SARS-CoV-2 spread, as it is an elective surgery and its delay does not determine additional risks for patients [ABSTRACT FROM AUTHOR] Copyright of BioMed Research International is the property of Hindawi Limited and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission However, users may print, download, or email articles for individual use This abstract may be abridged No warranty is given about the accuracy of the copy Users should refer to the original published version of the material for the full abstract (Copyright applies to all Abstracts )

Aims. We aimed to summarize available evidence about intraoperative and postoperative donors’ and recipients’ outcomes following stone surgery in renal grafts from living donors performed either before donation or as ex vivo bench surgery at the time of living-donor nephrectomy. Methods. A systematic review of PubMed, ISI Web of Knowledge, and Scopus databases was performed in September 2020. We included full papers that met the following criteria: original research, English language, human studies, and describing the results of stone surgery in renal grafts from living donors performed either before transplantation or as ex vivo bench surgery. Results. We identified 11 studies involving 106 patients aged between 22 and 72 years. Predonation and bench stone surgery was performed in 9 (8.5%) and 96 (90.6%) patients, respectively. Predonation stone surgery involved extracorporeal shock wave lithotripsy, retrograde intrarenal surgery, and percutaneous nephrolithotomy in 8, 1, and 1 patient, respectively. The overall success rate of predonation stone surgery was 78%, and the complication rate was 0%. Bench stone surgery involved ureteroscopy, pyelolithotomy, or a combination of both in 79 (82.3%), 10 (10.4%), and 7 (7.3%) cases, respectively, with an overall success rate of 95.8% and an overall complication rate of 9.37%. Conclusions. Predonation and bench stone surgery in grafts from living donors represents efficacious and safe procedures. Further studies on wider series with a longer follow-up are required.

The potential mechanisms of action of polyphenols in nonalcoholic fatty liver disease (NAFLD) are overlooked. Here, we evaluate the beneficial therapeutic effects of hydroxytyrosol (HT), the major metabolite of the oleuropein, in a nutritional model of insulin resistance (IR) and NAFLD by high-fat diet. Young male rats were divided into three groups receiving (1) standard diet (STD; 10.5% fat), (2) high-fat diet (HFD; 58.0% fat) and (3) HFD+HT (10 mg/kg/day by gavage). After 5 weeks, the oral glucose tolerance test was performed, and at 6th week, blood sample and tissues (liver and duodenum) were collected for following determinations. The HT-treated rats showed a marked reduction in serum AST, ALT and cholesterol and improved glucose tolerance and insulin sensitivity, reducing homeostasis model assessment index. HT significantly corrected the metabolic impairment induced by HFD, increasing hepatic peroxisome proliferator activated receptor PPAR-α and its downstream-regulated gene fibroblast growth factor 21, the phosphorylation of acetyl-CoA carboxylase and the mRNA carnitine palmitoyltransferase 1a. HT also reduced liver inflammation and nitrosative/oxidative stress decreasing the nitrosylation of proteins, reactive oxygen species production and lipid peroxidation. Moreover, HT restored intestinal barrier integrity and functions (fluorescein isothiocyanate-dextran permeability and mRNA zona occludens ZO-1). Our data demonstrate the beneficial effect of HT in the prevention of early inflammatory events responsible for the onset of IR and steatosis, reducing hepatic inflammation and nitrosative/oxidative stress and restoring glucose homeostasis and intestinal barrier integrity.

Horses affected by chronic piroplasmosis may develop poor performance and muscle atrophy. Here we investigate the pathological and immunopathological aspects of myopathy occurring in chronic equine piroplasmosis. The study included 16 horses serologically positive for equine piroplasms presenting with clinical signs and supporting serum biochemical evidence of a myopathy. Skeletal muscle was evaluated by histopathology, immunohistochemistry, indirect immunofluorescence, and molecular detection of piroplasms and inflammatory cytokines in skeletal muscle. Histologic lesions included muscle fiber atrophy (100% of cases), degenerative changes (13/16, 81%), and perivascular perimysial and endomysial lymphocytic infiltrates (81% of cases). In 15 cases (94%), muscle fibers had strong immunostaining for major histocompatibility complex classes I and II. T lymphocyte populations were mainly CD3+, CD8+, and CD4+ in equal proportions, with a lower number of CD79α+ cells. The serum from affected horses was tested by indirect immunofluorescence for binding of IgG, IgM, or IgA to sections of normal equine muscle to detect circulating autoantibodies against muscle antigen(s). In all cases, distinct sarcolemmal staining was detected in sections incubated with serum from affected horses, in contrast to sections incubated with phosphate-buffered saline or equine control sera. Reverse transcription polymerase chain reaction (RT-PCR) testing of muscles from affected animals revealed a significant increase of interferon-γ, interleukin-12, and tumor necrosis factor–α gene expression compared to healthy controls. Theileria equi or Babesia caballi was not detected in samples of affected muscle by RT-PCR. Thus, inflammatory myopathy associated with equine piroplasmosis may involve an autoimmune pathogenesis with upregulation of inflammatory cytokines that may cause myofiber atrophy and degeneration.

Background Autophagy is a highly regulated process involving the bulk degradation of cytoplasmic macromolecules and organelles in mammalian cells via the lysosomal system. Dysregulation of autophagy is implicated in the pathogenesis of many neurodegenerative diseases and integrity of the autophagosomal - lysosomal network appears to be critical in the progression of aging. Our aim was to survey the expression of autophagy markers and Amyloid precursor protein (APP) in aged bovine brains. For our study, we collected samples from the brain of old (aged 11–20 years) and young (aged 1–5 years) Podolic dairy cows. Formalin-fixed and paraffin embedded sections were stained with routine and special staining techniques. Primary antibodies for APP and autophagy markers such as Beclin-1 and LC3 were used to perform immunofluorescence and Western blot analysis. Results Histologically, the most consistent morphological finding was the age-related accumulation of intraneuronal lipofuscin. Furthermore, in aged bovine brains, immunofluorescence detected a strongly positive immunoreaction to APP and LC3. Beclin-1 immunoreaction was weak or absent. In young controls, the immunoreaction for Beclin-1 and LC3 was mild while the immunoreaction for APP was absent. Western blot analysis confirmed an increased APP expression and LC3-II/LC3-I ratio and a decreased expression of Beclin-1 in aged cows. Conclusions These data suggest that, in aged bovine, autophagy is significantly impaired if compared to young animals and they confirm that intraneuronal APP deposition increases with age.

Sarcopenia, the age-related loss of muscle mass and strength, is a multifactorial condition that represents a major healthcare concern for the elderly population. Although its morphologic features have been extensively studied in humans, animal models, and domestic and wild animals, only a few reports about spontaneous sarcopenia exist in other long-lived animals. In this work, muscle samples from 60 healthy Podolica-breed old cows (aged 15–23 years) were examined and compared with muscle samples from 10 young cows (3–6 years old). Frozen sections were studied through standard histologic and histoenzymatic procedures, as well as by immunohistochemistry, immunofluorescence, and Western blot analysis. The most prominent age-related myopathic features seen in the studied material included angular fiber atrophy (90% of cases), mitochondrial alterations (ragged red fibers, 70%; COX-negative fibers, 60%), presence of vacuolated fibers (75%), lymphocytic (predominantly CD8+) inflammation (40%), and type II selective fiber atrophy (40%). Immunohistochemistry revealed increased expression of major histocompatibility complex I in 36 cases (60%) and sarcoplasmic accumulations of β-amyloid precursor protein–positive material in 18 cases (30%). In aged cows, muscle atrophy was associated with accumulation of myostatin. Western blot analysis indicated increased amount of both proteins—myostatin and β-amyloid precursor protein—in muscles of aged animals compared with controls. These findings confirm the presence of age-related morphologic changes in cows similar to human sarcopenia and underline the possible role of amyloid deposition and subsequent inflammation in muscle senescence.

This paper is dedicated to the memory of our wonderful colleague Professor Alfredo Colonna, who passed away the same day of its acceptance. Fatty liver accumulation, inflammatory process and insulin resistance appear to be crucial in non-alcoholic fatty liver disease (NAFLD), nevertheless emerging findings pointed an important role also for iron overload. Here, we investigate the molecular mechanisms of hepatic iron metabolism in the onset of steatosis to understand whether its impairment could be an early event of liver inflammatory injury. Rats were fed with control diet or high fat diet (HFD) for 5 or 8 weeks, after which liver morphology, serum lipid profile, transaminases levels and hepatic iron content (HIC), were evaluated. In liver of HFD fed animals an increased time-dependent activity of iron regulatory protein 1 (IRP1) was evidenced, associated with the increase in transferrin receptor-1 (TfR1) expression and ferritin down-regulation. Moreover, ferroportin (FPN-1), the main protein involved in iron export, was down-regulated accordingly with hepcidin increase. These findings were indicative of an increased iron content into hepatocytes, which leads to an increase of harmful free-iron also related to the reduction of hepatic ferritin content. The progressive inflammatory damage was evidenced by the increase of hepatic TNF-α, IL-6 and leptin, in parallel to increased iron content and oxidative stress. The major finding that emerged of this study is the impairment of iron homeostasis in the ongoing and sustaining of liver steatosis, suggesting a strong link between iron metabolism unbalance, inflammatory damage and progression of disease.

Scant information is available on the ultrasonographic appearance of different testicular tumours in the stallion. Preoperative ultrasound imaging and gross and microscopic features of a testicular teratoma in a horse is described. An asymptomatic 4 years old cryptorchid Arabian horse was admitted for orchiectomy. Combined transabdominal and inguinal ultrasound examination revealed a large complex ovoid mass, containing both solid and cystic elements with internal echoes, located dorsally to the superficial inguinal ring. Two main hypoechoic cavities divided by a linear hyperechoic septum were evident, with a hyperechoic circular structure inside the lumen of the largest one. A tumour of the undescended testis was suspected. Ultrasound findings guided a provisional diagnosis of teratoma that was confirmed by histology following surgical removal of the tumour. Due to the correspondence between ultrasonographic and morphological features, trans-abdominal ultrasonography was conclusive in the preoperative planning.

Angiostrongylus vasorum (Nematoda: Angiostrongylidae) infection was detected at post-mortem examination in the pulmonary arteries and hearts of 34/102 (33,3%) of red foxes (Vulpes vulpes) from the Campania Region in southern Italy. Pathological changes consisted of granulomatous interstitial pneumonia caused by larvae and intravascular pulmonary adult nematodes. These changes confirm that angiostrongylosis infection in red foxes has a mainly chronic course, in which the infected host may disperse parasite larvae in the environment over its lifetime. Results suggest that the life cycle of A. vasorum is well established in the red fox in the Campania Region representing a potential infection risk for dogs.

Background: Canine angiostrongylosis is a nematode infection in domestic dogs and wild carnivores. The present report focuses on epidemiological, clinical and histopathological findings in a case of fatal disseminated angiostrongylosis in a dog living in southern Italy and provides data on the extent of the spread of Angiostrongylus vasorum in the same area.Case presentation: A 4-year-old female English Setter from the Campania region of southern Italy was referred with a 2-week history of cough and severe respiratory distress that did not respond to antimicrobial therapy. Based on clinical, radiological, echographical and cytological findings (including the presence of larvae), a suspect diagnosis of lungworm infection was performed. After few days the dog died due to progressive clinical aggravation. Complete postmortem examination was conducted within 24 hours from death and samples from lungs, heart, liver, kidney, spleen, stomach and small intestine were fixed in 10% buffered formalin. Grossly, several hemorrhagic foci were observed mostly in the lungs, liver, kidney. Microscopically, the lungs contained numerous, multifocal to coalescing granulomas composed of epitheliod macrophages, multinucleated giant cells and some neutrophils, frequently associated with parasite eggs and larvae. The lungs contained many firm nodules, many adult nematodes approximately 1.5 to 2 cm in length were observed in cut sections and identified as A. vasorum. A subsequent parasitological survey performed with FLOTAC on stray dogs living in the same area showed the presence of A. vasorum larvae in 17 of 1639 stray dogs examined (1.04%).Conclusion: This survey provides new data on distribution of A. vasorum and underlines that canine angiostrongylosis should be considered as differential diagnosis in dogs.

AIMS/HYPOTHESIS: The aim of this study was to investigate the function of Prep1 (also known as Pknox1) in hepatic lipogenesis. METHODS: The hepatic lipogenesis pathway was evaluated by real-time RT-PCR and Western blot. Biochemical variables were assessed using a clinical chemistry analyser. RESULTS: Serum triacylglycerols and liver expression of fatty acid synthase (FAS) were significantly decreased in Prep1 hypomorphic heterozygous (Prep1 (i/+) ) mice compared with their non-hypomorphic littermates. Upstream FAS expression, phosphorylation of protein kinase C (PKC)?, liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) increased in Prep1 (i/+) mice, while protein and mRNA levels of the lipid phosphatase inhibitor of PKC?, SH2-containing inositol 5'-phosphatase 2 (SHIP2), was more than 60% reduced. Consistent with these findings, HepG2 cells transfected with Prep1 cDNA exhibited increased triacylglycerol accumulation and FAS expression, with strongly reduced PKC?, LKB1, AMPK and ACC phosphorylation. Further experiments revealed the presence of both Prep1 and its major partner Pbx1 at the Ship2 (also known as Inppl1) promoter. PBX-regulating protein 1 (PREP1) and pre-B cell leukaemia transcription factor 1 (PBX1) enhanced Ship2 transcription. The PREP1HR mutant, which is unable to bind PBX1, exhibited no effect on Ship2 function, indicating transcriptional activation of Ship2 by the PREP1/PBX1 complex. Treatment with a methionine- and choline-deficient diet (MCDD) induced steatosis in both Prep1 (i/+) and non-hypomorphic control mice. However, alanine aminotransferase increase, intracellular triacylglycerol content and histological evidence of liver steatosis, inflammation and necrosis were significantly less evident in Prep1 (i/+) mice, indicating that Prep1 silencing protects mice from MCDD-induced steatohepatitis. CONCLUSIONS/INTERPRETATION: Our results indicate that Prep1 silencing reduces lipotoxicity by increasing PKC?/LKB1/AMPK/ACC signalling, while levels of PREP1 expression may determine the risk of steatohepatitis and its progression.